Pathophysiology
Summary
Chronic kidney disease (CKD) is a progressive disorder characterized by decreased glomerular filtration rate (GFR) and kidney damage. Histopathologically, CKD-affected kidneys show bilaterally shrunken morphology with a red-brown, diffusely granular surface, glomerular scarring & interstitial fibrosis, as well as waxy casts in the urine.
The most prevalent etiologies of CKD are chronic hypertension (most common) and poorly controlled diabetes, both of which cause microvascular damage and chronic alteration of glomerular hemodynamics. Other causes include chronic glomerulonephritis, polycystic kidney disease, bilateral renal artery stenosis (ischemic nephropathy), and chronic pyelonephritis (fibrotic scarring).
CKD leads to a host of systemic complications. These include hypertension (volume overload), normocytic anemia (reduced renal EPO production), and hyperphosphatemia (decreased renal excretion). CKD results in hypovitaminosis D (impaired 1-alpha-hydroxylase activity), which contributes to the development of hypocalcemia. CKD can also induce secondary hyperparathyroidism, as hypocalcemia stimulates PTH release, leading to CKD-mineral and bone disorder (CKD-MBD) manifesting as either osteitis fibrosa cystica or osteomalacia.
Uremia, marked by increased blood urea nitrogen (BUN), causes GI, hematological, and neurological complications ranging from nausea and platelet dysfunction to encephalopathy and seizures. Additionally, CKD is an independent risk factor for developing coronary artery disease.
CKD is staged into 5 stages defined by GFR, with stage 5 signifying end-stage renal disease necessitating dialysis. Diagnostically, it is confirmed by 3 months of reduced GFR or albuminuria.
Lesson Outline
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FAQs
Chronic kidney disease (CKD) is a progressive disorder characterized by impaired kidney function over an extended period. Clinically, the kidneys may appear bilaterally shrunken and exhibit a red-brown, granular surface. The hallmark laboratory findings include a reduced glomerular filtration rate (GFR), elevated serum creatinine, and albuminuria—indicative of renal damage.
CKD is an independent risk factor for developing coronary artery disease. The disease can lead to hypertension due to volume overload, and metabolic imbalances like hyperkalemia can further stress the cardiovascular system. Additionally, uremia, a condition associated with advanced CKD, can cause platelet dysfunction leading to pathologic hemorrhage, further complicating cardiovascular health.
The most common causes of CKD include poorly controlled diabetes and chronic hypertension, both of which lead to microvascular damage in the kidneys. Other causes can be chronic glomerulonephritis, polycystic kidney disease, bilateral renal artery stenosis due to ischemic nephropathy, and chronic pyelonephritis resulting from progressive renal scarring.
CKD is diagnosed by 3 months of reduced GFR or elevated urine albumin. The initial injury leading to CKD causes the remaining healthy glomeruli to increase filtration to preserve GFR (adaptive hyperfiltration), which eventually leads to their damage due to the extra load, and labs start to show signs of CKD.
CKD can lead to a range of complications including metabolic acidosis, hyperkalemia, and fluid retention, which can lead to edema and hypertension. It can also cause normocytic anemia due to decreased erythropoietin production and various bone mineral disorders like osteitis fibrosa cystica and osteomalacia. Neurological symptoms such as peripheral neuropathy and encephalopathy, as well as gastrointestinal symptoms like nausea and vomiting, can also occur due to uremia.
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